Abstract
Molecular mechanisms responsible for periodontal disease (PD) and its worsening in type 1 Diabetes Mellitus (DM1) remain unknown. Cytokine profile and expression levels of collagenases, Mmp14, and tissue inhibitors were determined, as were the numbers of neutrophils and macrophages in combined streptozotocin-induced DM1 and ligature-induced PD models. Increased IL-23 (80-fold) and Mmp8 expression (25-fold) was found in DM1. Ligature resulted in an IL-1β/IL-6 profile, increased expression of Mmp8, Mmp13, and Mmp14 (but not Mmp1), and transient expression of Timp1 and Reck in non-diabetics. PD in DM1 involved IL-1β (but not IL-6) and IL-23/IL-17, reduced IL-6 and IL-10, sustained Mmp8 and Mmp14, increased Mmp13 and reduced Reck expression in association with 20-fold higher counts of neutrophils and macrophages. IL-23 and Mmp8 expression are hallmarks of DM1. In association with the IL-1/IL-6 (Th1) response in PD, one found a secondary IL-17 (Th17) pathway in non-diabetic rats. Low IL-6/TNF-α suggest that the Th1 response was compromised in DM1, while IL-17 indicates a prevalence of the Th17 pathway, resulting in high neutrophil recruitment. Mmp8, Mmp13, and Mmp14 expression seems important in the tissue destruction during PD in DM1. PD-associated IL-1/IL-6 (Th1), IL-10, and Reck expression are associated with the acute-to-chronic inflammation transition, which is lost in DM1. In conclusion, IL-23/IL-17 are associated with the PD progression in DM1.
Copyright © 2011 Wiley Periodicals, Inc.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alveolar Bone Loss / enzymology
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Alveolar Bone Loss / etiology
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Alveolar Bone Loss / immunology
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Animals
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Diabetes Mellitus, Experimental / complications*
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Diabetes Mellitus, Experimental / enzymology
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Diabetes Mellitus, Experimental / genetics
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Diabetes Mellitus, Experimental / immunology
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Diabetes Mellitus, Type 1 / complications*
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Diabetes Mellitus, Type 1 / enzymology
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Diabetes Mellitus, Type 1 / genetics
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Diabetes Mellitus, Type 1 / immunology
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Disease Progression
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GPI-Linked Proteins / metabolism
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Gingiva / enzymology*
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Gingiva / immunology*
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Inflammation Mediators / metabolism*
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Interleukin-10 / metabolism
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Interleukin-17 / metabolism*
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Interleukin-1beta / metabolism
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Interleukin-23 / metabolism*
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Interleukin-6 / metabolism
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Ligation
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Macrophages / immunology
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Male
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Matrix Metalloproteinase 13 / metabolism
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Matrix Metalloproteinase 14 / genetics
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Matrix Metalloproteinase 14 / metabolism*
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Matrix Metalloproteinase 8 / genetics
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Matrix Metalloproteinase 8 / metabolism*
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Molar / surgery
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Neutrophil Infiltration
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Neutrophils / immunology
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Periodontal Diseases / complications*
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Periodontal Diseases / enzymology
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Periodontal Diseases / genetics
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Periodontal Diseases / immunology
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RNA, Messenger / metabolism
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Rats
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Rats, Wistar
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Th17 Cells / immunology
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Time Factors
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Tumor Suppressor Proteins / metabolism
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Up-Regulation
Substances
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GPI-Linked Proteins
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Il17a protein, rat
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Inflammation Mediators
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Interleukin-17
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Interleukin-1beta
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Interleukin-23
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Interleukin-6
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RNA, Messenger
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Reck protein, rat
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Tumor Suppressor Proteins
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Interleukin-10
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Matrix Metalloproteinase 13
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Mmp13 protein, rat
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Matrix Metalloproteinase 8
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Matrix Metalloproteinase 14